This laboratory has established that the pattern of T helper cell (Th) dysfunction seen in asymptomatic, HIV-seropositive (HIV+) is also detected in patients with systemic lupus erythematosus (SLE), and in two murine models of SLE. These two induced murine models of SLE were compared for the genetics of resistance and susceptibility. Both the parent T cell into F1 murine chronic graft-vs-host disease (cGVHD) and the 16/6 Id SLE-induced models mapped genetic susceptibility to genes on chromosomes 7 and 14. These findings indicate that SLE induced by two completely different protocols and mechanisms results in control of resistance and susceptibility by the same genes. A mechanistic common denominator was also discovered in that the 16/6 Id model requires immunization with the human SLE 16/6 Id antibody, whereas cGVHD stimulates endogenous production of 16/6 Id, resulting in SLE disease. By using different F1 hybrid and parental mouse strain combinations, we demonstrated that the Mls locus and not the MHC determines whether parental T lymphocytes inoculated into F1 recipients will induce chronic or acute graft-vs-host disease, and that certain models of GVHD appear to start out as acute and then shift to a chronic form. - AIDS like, autoantibodies, autoimmunity, gp, 0, lupus, - Human Tissues, Fluids, Cells, etc.